Cardiovascular Flashcards
1
Q
What is angina?
A
Chest pain when blood flow to coronary arteries is restricted. It is a symptom of restricted blood flow.
2
Q
What is the main cause of angina?
A
Atherosclerosis
3
Q
What are the 3 main coronary arteries?
A
Right coronary artery
Circumflex artery
Left anterior descending
4
Q
What is Pouiselle’s law?
A
Resistance α 1/radius^4
5
Q
In a healthy individual at rest is the resistance of the epicardial vessels and microvasculature low medium or high?
compared to a diseased individual at rest?
A
Epicardial vessels = low
Microvasculature = medium
Diseased-
Epicardial vessels = high
Microvasculature = lower(compensating)
6
Q
What is the average flow rate of blood in coronary arteries? and what can it increase to in exercise?
A
3ml/s
Above 15ml/s
7
Q
What are the main non modifiable risk factors for angina?
A
Gender, age, family history
8
Q
What are the main modifiable risk factors for angina?
A
Smoking, hypertension, diabetes, hypercholesterolaemia, sedentary lifestyle, stress(less)
9
Q
What is the main clinical feature of angina?
A
Chest pain
10
Q
What are the 3 key points used to score angina /3?
A
- Central heavy pain, tight/radiating to arm/jaw/neck
- Pain precipitated by exertion
- Pain relieved by rest
3/3 = typical angina
2/3 = atypical pain
1 or less/3 = non anginal pain
11
Q
What are the main differential diagnoses of angina?
A
Pericarditis/PE/pleurisy/chest infection/ dissection of aorta
12
Q
On examination how may a patient with stable angina present?
A
Often normal
13
Q
What ‘sign’ do you look out for in patients with angina?
A
Levine sign (clenched fists over chest)
14
Q
What are the two basic investigations done when a patient has suspected angina and what is seen?
A
- ECG - Can be normal (between attacks) or show resting ST segment depression/ T wave flattening or inversion
- Echo - often normal. May be signs of previous infarcts, long Q waves, T wave inversion, BBB
15
Q
What is the definition of hypertension? (value)
A
140/90mmHg based on at least two readings on separate occasions/ ambulatory blood pressure monitoring (24 hrs)
16
Q
Hypertension is a major risk factor for what?
A
Stroke, MI, HF, renal disease, cognitive decline
Also increases risk of AF
17
Q
Give the equation for blood pressure
A
BP = CO x TPR
18
Q
What two factors play a big role in determining CO and TPR and therefore blood pressure?
A
- Renin-angiotensin-aldosterone system
2. Sympathetic nervous system(NA)
19
Q
What affect does Angiotensin II have on the systemic circulation?
A
Potent vasoconstrictor
20
Q
What effect does aldosterone have on tubular reabsorption/excretion of ions?
A
Reabsorbs sodium and chloride
Secretes potassium
21
Q
How do ACE - inhibitors work?
A
Reduce convertion of angiotensin I to angiotensin II
22
Q
What conditions are ACE-inhibitors used in?
A
- Hypertension
- Heart failure
- Diabetic neuropathy
23
Q
What conditions are ACE-inhibitors contraindicated in?
A
Renal artery stenosis and preganacy (teratogenic)
24
Q
Give 2 examples of ACE-inhibitors?
A
Ramipril, enalapril
25
What are the adverse effects of ACE-inhibitors?
1. Decrease in angiotensin II causes hypotension, vasodilation of efferent arteriole and therefore acute renal failure, hyperkalaemia and is teratogenic
2. Increased kinin production causes a dry cough in 10%, a rash and anaphylactoid reaction
26
Why do ACE inhibitors cause increase kinin production, and what effect does this have on systemic circulation?
ACE converts angiotensin I --> angiotensin II alongside bradykinin being converted into inactive peptides, so builds up as is no longer being converted
Bradykinin is a vasodilator
27
What is the main cause for the use of angiotensin II receptor blockers? (ARB)
If ACE-inhibitor contraindicated (i.e. causes a cough)
28
In what conditions are ARB's used in?
1. Hypertension
2. HF
3. Diabetic neuropathy
29
Give 2 examples of ARB's
1. Losartan
| 2. Candesartan
30
What are the main adverse effects of ARB's?
1. Symptomatic hypotension
2. Hyperkalaemia
3. Potential renal dysfunction
4. Rash
5. Angioedema (result of allergic reaction)
6. CONTRAINDICATED IN PREGNANCY
31
How do angiotensin II receptor blockers (antagonists) work?
Selectively block receptor for angiotensin II (AT-1 receptor) meaning little aldosterone production.
32
What conditions are calcium channel blockers used in?
1. Hypertension
2. IHD (angina)
3. Arrhythmia (tachy)
33
How do calcium channel blockers work?
Block L-type calcium channels and modify calcium uptake into myocardium and vascular smooth muscle.
Dihydropyridines are potent vasodilators with little effect on cardiac contractility or conduction
Verapamil/diltiazem are weak vasodilators but depress cardiac conduction and contractility
34
What are the 3 classes of calcium channel blockers and give at least one example of each alongside how they work
Dihydropyridines: Vasodilator e.g. amlodipine, nifedipine, felodipine
Phenylalkylamines: Negatively inotropic and chronotropic e.g. verapamil
Benzothiazepines: Intermediate heart and peripheral vascular effects e.g. diltiazem
35
Define chronotropic and inotropic
Chronotropic- Alters heart rate
| Inotropic - Alters force or energy of cardiac contraction
36
What are the adverse effects of calcium channel blockers (calcium antagonists)?
1. Due to peripheral vasodilation: flushing, oedema, headache, palpitations (dihydropyridines)
2. Due to negatively chronotropic effects: Bradycardia, AV block (verapamil/ diltiazem)
3. Due to negatively inotropic effects: worsening HF (verapamil/diltiazem)
Verapamil can also cause constipation
37
How do beta blockers work?
They block the B-adrenoreceptors in the heart, peripheral vasculature, bronchi, pancreas and liver.
This decreases heart rate (negatively chronotropic) Reduces the force of cardiac contraction (negatively inotropic) - reduce myocardial oxygen demand and give more time for perfusion
Lowers blood pressure
38
In what conditions are beta blockers used?
1. IHD (angina)
2. HF
3. Arrhythmia
4. Hypertension
39
Which beta blockers are classified as B1 selective?
Metoprolol
| Bisoprolol (potentially atenolol but is more central)
40
Which beta blockers are classified as non selective?
Propanolol
Nadolol
Carvedilol
41
What happens to the selectivity of beta blockers at high doses?
Selectivity is lost
42
What is meant by the term 'cardioselective'?
Implies B1 selectivity
| However, up to 40% of cardiac B-adrenoreceptors are actually B2 receptors
43
What are the main adverse effects of beta blockers?
1. Fatigue, headache, sleep disturbance/nightmares
2. Bradycardia, hypotension, cold peripheries, erectile dysfunction
3. Worsening of asthma, PVD, HF (if given standard dose/acutely)
44
In what conditions are beta blockers contraindicated?
```
Asthma
HF (in standard dose- if given in v.v. small doses is actually the treatment of HF)
```
45
How do diuretics work?
Reduce sodium and chloride reabsorption at different sites in the nephron and thus increase urinary sodium and water loss.
46
In what conditions are diuretics used?
1. Hypertension
| 2. Heart failure
47
What are the 3 classes of diuretic and how do they work?
1. Thiazides + related (distal tubule also reduce peripheral vascular resistance)
2. Loop diuretics (loop of Henle and increase venous capacitance (helps acute HF))
3. Potassium sparing diuretics/aldosterone receptor antagonist - don't cause hypokalaemia so can be used in conjunction with loop or thiazide diuretics
48
Give an example of each of a drug in each of the 3 main classes of diuretics
1. Thiazides - Bendroflumethiazide
2. Loop diuretics - Furosemide
3. Potassium sparing/aldosterone antagonist - Spironolactone
49
What are the main adverse effects of diuretics?
1. Hypovolaemia or hypotension (loop)
2. Low serum potassium, sodium, magnesium, calcium
3. Raised uric acid (can lead to gout)
4. Erectile dysfunction (thiazides)
5. Impaired glucose tolerance (thiazides)
50
What are the 3 classes of antihypertensives that are
| smaller and give an example of each
1. Alpha-1 adrenoreceptor blockers (doxazosin)
2. Centrally acting antihypertensives (methyldopa)
3. Direct renin inhibitor (aliskiren)
51
Patient under 55 presents with hypertension. What is the first step taken in their treatment?
ACE inhibitor (or ARB)
52
Patient aged 55 or over presents with hypertension. What is the first step taken in their treatment?
Calcium channel blocker
53
43 year old afro-Caribbean patient presents with hypertension. What is the first step taken in their treatment?
Calcium channel blocker
54
Patient with hypertension presents, they have had first stage treatment but it hasn't been effective. What happens now?
Prescribe ACE inhibitor/ARB and calcium channel blocker
55
Patient presents with hypertension. They are currently on both a ACE inhibitor and a calcium channel blocker. What is the next step in their treatment?
Add a thiazide like diuretic
56
Patient presents with hypertension. They are currently on ACE inhibitor, calcium channel blocker and thiazide like diuretic. What is the next step in their treatment?
Add either:
| Spironolactone, alpha blocker, beta blocker or high dose thiazide like diuretic
57
What is heart failure?
Complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired
58
What are the two types of heart failure and which is the most common?
HF due to left ventricular systolic dysfunction (LVSD)
HF due to preserved ejection fraction (diastolic failure) (HFPEF)
Most common is LVSD
59
What is the most common cause of HF?
Coronary artery disease
60
In heart failure, what has been shown to be the most useful type of therapy?
Neurohumoral blockade (RAAS-SNS) - blocking these
NOT/ Direct LV stimulation
61
In HF, what class of drugs are prescribed to treat congestion?
Diuretics (usually loop)
62
Alongside diuretics (to treat congestion) what would be the first line of treatment in a patient with HF?
ACE inhibitor + beta blocker (low dose and very slow uptitration)
63
What drug or combination of drugs would be used in a patient with heart failure if they were both ACE-I and ARB intolerant?
Hydralazine/nitrate combination
64
What hormones are released by the heart when atrial and ventricular muscle cells are stretched or there is raised atrial and ventricular pressure?
Atria - Atrial natriuretic peptide
| Ventricles - Brain natriuretic peptide
65
What are the main effects of the hormones ANP and BNP released by the heart?
1. Increase renal excretion of sodium and water
2. Relax vascular smooth muscle (except efferent arterioles)
3. Increased vascular permeability
4. Inhibits release or effects of aldosterone, angiotensin II, endothelin and ADH
66
What hormones work against the renin angiotensin system?
Cardiac natriuretic peptides
67
How can levels of cardiac natriuretic peptides be manipulated to provide therapy for heart failure?
CNP's are metabolised by NEP (neprilysin)
NEP inhibition increases their levels
Entresto does this
68
How do nitrates work and what conditions do they treat?
Are arterial and venous dilators, so reduce preload and afterload
Lower BP
Used in IHD (angina) and HF
69
What are the main side effects of nitrates?
Headache, GTN syncope
70
What are the main differences between chronic stable angina and unstable angina?
Chronic stable = occurs on exertion, infrequent
| Unstable = unpredictable, frequent, may occur at rest
71
What classes of drugs would you prescribe in chronic (stable) angina?
1. Antiplatelet therapy (aspirin or clopidogrel)
2. Lipid-lowering therapy - statins (simvastatin)
3. Short acting nitrate (acute attack) - GTN
4. First line treatment for cause of angina - Beta blocker or calcium channel blocker
72
What classes of drugs would you prescribe in acute coronary syndromes? (NSTEMI and STEMI)
1. Dual antiplatelet therapy (Aspirin + clopidogrel)
2. Lipid lowering therapy (statin)
3. Antithrombin therapy: Fondaparinux
4. Background angina therapy - BB, CCB
5. Pain relief- GTN spray and opiates (diamorphine)
6. HIGH RISK- Glycoprotein inhibitor (tirofiban)
7. Therapy for LVSD as req'd - ACE-I, BB, Aldosterone antagonist
73
What are the 4 main classes of antiarrhythmic drugs?(Vaughan Williams classification)
Class 1: Sodium channel blockers
Class 2: Beta adrenoreceptor antagonists
Class 3: Prolong AP (amiodarone)
Class 4: Calcium channel blockers (verapamil, diltiazem)
74
What are the two most prevalent causes underlying coronary thrombosis?
1. Plaque rupture
| 2. Plaque erosion
75
What are the major cell types involved in atherosclerosis?
Endothelium, macrophages, smooth muscle cells and platelets
76
What are the risk factors for atherosclerosis?
Age, tobacco smoking, high serum cholesterol, obesity, diabetes, hypertension, family history
77
What are the 3 factors involved in Virchow's triad?(thrombosis)
1. Endothelial injury
2. Hypercoagulability
3. Stasis of blood flow (changes)
78
How is inflammation on the arterial wall ignited?
LDL's accumulate on the wall and are modified by oxidation.
This inflames endothelial cells
Endothelial cells then release chemoattractants which attract macrophages, which are transmigrated into intima.
79
What is the term used for the first signs of atherosclerosis. What cells do these lesions include?
Fatty streaks
| Include lipid laden macrophages (foam cells) and T lymphocytes in intima
80
How are intermediate lesions in atherosclerosis different from fatty streaks?
Include vascular smooth muscle cells from media.
| Also have platelets beginning to aggregate to them
81
What is the term given to lipid laden macrophages in atherosclerosis?
Foam cells
82
The fibrous cap formed in advanced lesions of atherosclerosis is made from extracellular matrix proteins (collagen and elastin). What cells lay down this fibrous cap?
Smooth muscle cells
83
Why must the fibrous cap be resorbed and redeposited in order to be maintained?
Is a balance between T lymphocytes interacting with macrophages and resorbing the cap, and new collagen and elastin being layed down by smooth muscle cells
84
How are advanced lesions in atherosclerosis different to both intermediate lesions and fatty streaks?
Include a fibrous cap made of elastin and collagen (+ other ECM cells)
85
What is the difference between plaque erosion and plaque rupture?
Thrombus in plaque rupture is red vs. in plaque erosion is white (neutrophils)
Plaque erosion is not assosciated with high cholesterol (LDL) and the fibrous cap is not disrupted
However mechanism is unknown
86
What does PCI stand for and what is the main form of PCI treatment?
Percutaneous coronary intervention
Stenting
87
If an electrical wave of depolarisation is travelling towards an electrode what kind of deflection is seen?
Positive (opposite if is a wave of repolarisation)
88
State the 5 steps of impulse conduction in the heart beginning at SA node
1. Sinoatrial node
2. AV node
3. Bundle of His
4. Bundle branches
5. Purkinje fibres
89
Why can the T wave not normally be seen on an ECG?
Occurs at the same time as QRS
90
What is the PR interval?
Start of P to start of QRS
Is the atrial depolarisation + delay in the AV junction (AV node to bundle of His)- this allows for the atria to contract before ventricles
91
What is the QT interval?
Start of Q until end of T
92
What is the difference between limb leads and precordial leads?
The limb leads are bipolar, so is measuring the difference in electrical potential between these two points
The precordial leads are all placed around the heart and are unipolar leads, their electrical potential is compared to that of a virtual reference point (0) in the centre of the heart
93
What is the difference between standard limb leads and augmented limb leads?
Augmented limb leads use the same electrodes as standard limb leads, but instead of the negative pole being a single electrode, it is a combination of both of the remaining electrodes.
94
What do aVL, aVR and aVF stand for?
```
aVL = augmented vector left
aVR = augmented vector right
aVF = augmented vector foot
```
95
Where are each of the 6 precordial electrodes placed?
V1 4th intercostal space right of sternum
V2 4th intercostal space left of sternum
V3 Between V2 and V4
V4 5th intercostal space mid clavicular line
V5 Horizontal with V4 anterior axillary line
V6 Horizontal with V4 and V5 mid axillary line
96
What are the 10 rules in an ECG?
1. QRS should be less than 3 small squares <110ms
2. QRS should be dominantly upright in leads I and II
3. QRS and T waves should be in the same direction in all limb leads
4. P waves should be upright in leads I, II, V2-6
5. PR segment should be between 3 and 5 small squares (120-200ms)
6. T waves should be upright in leads I,II and V2-6
7. ST segment should be isoelectric or slightly elevated in V1-2
8. R wave should grow between V1-V4 and S wave should grow between V1 and V3 and not be present in V6
9. There should be no Q wave in leads I,II or v2-6 (or less than 1 small square)
10. All aVR waves should be negative
97
On ECG, P wave appears bifid or notched. What is this an indication of?
P.mitrale = Left atrium enlargement
Can be caused to mitral stenosis (narrowing of valve) or hypertension (systemic)
98
On ECG, P wave appears tall and peaked (>2.5mm). What is this an indication of?
P.pulmonale = Right atrium enlargement
Due to pulmonary hypertension or COPD/emphysema
99
If on ECG there is a short PR interval, what condition may the individual have?
Wolff-Parkinson-White syndrome
Has an accessory 'bundle of Kent' which allows early excitation of the ventricle
Individual may have bouts of tachycardia
100
What is a long PR interval suggestive of?
First degree heart block
101
If there is no initial downwards dip in the QRS segment, what is the first peak called?
R
102
What is a broad QRS complex suggestive of? >2.5 squares
Bundle branch block
103
If a patient had left ventricular hypertrophy what would been seen on their ECG?
Tall R waves in LV leads (v5+6) or deep S waves in RV leads (v1+2)
Sum would be greater than 40mm
104
If a patient had right ventricular hypertrophy what would be seen on their ECG?
Tall T waves in RV leads (v1+2) or deep S waves in LV leads (v5+6)
Sum would be greater than 40mm
105
ST segment is normally isoelectric
What does it suggest if not?
```
Elevation = MI/acute pericarditis
Depression = Ischaemia
```
>1mm
106
What is the QT interval, what is a normal QT interval and what does long QT interval give an increased risk of?
Start of QRS to end of T
Normal = 0.35-0.45 seconds
Long QT syndrome = increased risk of torsades de pointes and sudden death
107
Explain the two methods you can use to work out heart rate from an ECG
1. Rule of 300- for regular rhythms. Count number of big boxes between QRS and divide 300 by this
2. 10 second rule - for irregular beats - ECG's record 10 seconds of rhythm per page, so count number of beats present and x 6
108
What does the QRS axis represent?
The overall direction of the heart's electrical activity
109
What does a normal QRS axis range from and to?
-30 degrees to +90 degrees
110
What is left axis deviation?
-30 degrees to -90 degrees
111
What is right axis deviation?
+90 degrees to +180 degrees
112
If an M or W is seen in ECG in leads V1 or V6 what is it suggestive of ?
M v1 = RBBB
| M in v6 = LBBB
113
What are you looking for on ECG during a treadmill test to confirm angina/ stable CAD
ST segment depression
114
A CT angiogram has a high NPV and a low PPV. What does this mean it is useful in?
Good for exclusing CAD in younger, lower risk patients.
115
How would a positive stress echo appear on screen?
One side of the heart may stop working as much as the other
116
How does SPECT work?
1. Stress heart using drug (adenosine) and insert tracer- is taken up by metabolising tissues
2. Look at scan, if there is a perfusion defect then bring back for a second scan under resting conditions
3. If the perfusion defect goes on rest then it shows ischaemia, but if it remains is likely to be a scar
117
What tool is used to predict the 10 year risk of a major CV event?
SCORE
118
Name 3 categories of drugs that are first line antianginals
1. Beta blockers
2. Nitrates
2. Calcium channel blockers
119
What is the difference between primary and secondary prevention?
Primary prevention consists of risk factor modification, before a CV event occurs
Secondary prevention takes place after a CV event has occurred, in an attempt to prevent another as well as manage symptoms.
120
Why are calcium channel antagonists used as first line antianginals alongside beta-blockers and nitrates?
Are ARTERODILATORS (lowers blood pressure) (dihydropyridines)
Meaning that the afterload (pressure against which LV must pump to eject blood) is reduced
So reduce work of the heart and O2 demand
Verapamil/diltiazem are directly negatively inotropic
121
Why are beta blockers used as first line antianginals alongside calcium channel antagonists and nitrates?
Bind to B1 adrenoreceptors, in heart and are negatively chronotropic and inotropic
122
Why are nitrates used as first line antianginals alongside calcium channel blockers and beta blockers?
Nitrates are venodilators
Dilate systemic veins and so reduce venous return to R of heart
Reduces preload so via Frank Starling can see that work of heart is reduced
123
What are the main two categories of drugs that will actively decrease prognosis of a CV event in an individual that suffers with angina?
1. Antiplatelets (e.g. aspirin)
| 2. Statins (e.g. simvastatin)
124
How does aspirin work as antiplatelet therapy as well as an an analgesic?
It inhibits COX-1 which inhibits platelet generation of thromboxane-A2 at lower doses
At higher doses it binds and inactivates COX-1 and 2, which blocks prostaglandin production, having an analgesic effect.
125
What are the two methods of revascularisation and are the main pros and cons of each?
1. PCI - less invasive, fast recovery time but possibility of restenosis and need dual antiplatelet therapy
2. CABG- Long recovery, invasive, but can deal with complex disease and has good prognosis
126
What 2 things classify angina as unstable?
1. Cardiac chest pain at rest
2. Cardiac chest pain with crescendo pattern
3. New onset angina
127
What is the significance of a positive troponin test?
Suggests an MI in last 6 hours-2 weeks
| or other cardiac damage
128
What clinical findings would suggest a larger infarct and therefore a higher chance of pathological Q wave formation, heart failure and death?
ST elevation
| LBBB
129
ST elevation is suggestive of what?
MI - in aVL can also be caused by pericarditis
130
What are the classic symptoms of MI?
1. Unremitting cardiac chest pain (occurring at rest)
2. Sweating
3. Breathlessness
4. Nausea and vomiting
131
Why does heart failure cause salt and water retention (and therefore oedema)?
Low renal perfusion
132
Define pericardial tamponade
When fluid builds up in the pericardium and results in pressure on the heart
133
What in the normal amount of fluid in the pericardium, and what is the pericardium made from?
50ml
Acellular collagen and elastin fibres
134
What is the purpose of pericardium?
Restrains filling volume of heart
135
What are the main causes of hypertension?
85% of people it is unknown
10% due to hyperaldosteronism
5% kidney disease, drugs, rare hormone excreting tumours
136
If a patient presents with hypertension and hypokalaemia what is the most likely cause of the hypertension?
Hyperaldosteronism - potentially due to drugs
137
What is the standard fall in blood pressure seen with the patient on one antihypertensive?
9mmHg
138
How can a patient's home BP be measured?
24 hour ambulatory blood pressure monitoring
139
What is the threshold for requiring antihypertensive drugs in a patient with high blood pressure?
Depends on their risk
For low risk groups 160/100
For high risk groups 140/90
140
What symptom is supposed to be dulled down by antihypertensive medication in a patient with high blood pressure?
Headache
141
What BP are you aiming to achieve with medication and lifestyle changes in a hypertensive patient?
140/90 but tighter in diabetics
142
How many drugs does it usually take in combination to achieve a 'normal' blood pressure in a hypertensive patient?
2-4
143
What illnesses can be caused by HBP?
Dementia, stroke, peripheral vascular disease, aneurysm, renal failure, cardiovascular disease
144
On average how much does hypertension shorten a patient's life by?
7 years
145
What is the percentage reduction in chance of having a stroke per 10mmHg dropped in blood pressure?
40%
146
What are the main methods of lowering blood pressure without drug treatment?
1. Reduce salt intake
2. Lose weight
3. Reduce alcohol consumption
147
What are the main types of antihypertensive drugs?
A. ACE-I/ARB
B. Beta blocker
C. Calcium channel blocker
D. Diuretics
148
What factors (unrelated to lifestyle) may contribute to high blood pressure?
Drugs (prescribed or not)
- NSAIDs
- COPC
- SNRI's (antidepressants)
- Corticosteroids
- Cold cures
Or/ recreational
- Cocaine
- Amphetamines
149
In what circumstances should blood pressure lowering medication be withheld in a hypertensive patient?
Surgery
150
How often should you monitor the blood pressure of a previously hypertensive patient on antihypertensive medication?
Every 6-12 months
151
What are the 3 causes of aortic valve stenosis?
1. Degeneration and calcification of normal valve
2. Calcification of a congenital bicuspid valve
3. Rheumatic heart disease
152
How does aortic stenosis lead to angina, arrythmia and left ventricular failure?
Obstruction of left ventricular emptying, meaning increased afterload and so left ventricular hypertrophy.
This increases oxygen demand of heart until supply no longer meets demand and heart becomes ischaemic.
153
How can aortic stenosis present?
1. Angina
2. Syncope
3. Dyspnoea (and other symptoms of congestive HF) - most common symptom
154
How severe must aortic stenosis be before symptoms present?
Orifice is normally 1/4 of normal size
155
Explain why syncope is occasionally seen on exertion in patients with aortic stenosis
On exertion substances such as lactic acid and CO2 build up in muscles, stimulating parasympathetic nervous system to dilate vessels to allow more oxygen there, however this decreases blood pressure
CO can then not keep up with this vasodilation and individual loses consciousness
156
What investigation is often diagnostic in aortic stenosis?
Echo
-Doppler examination of valve allowes assessment of pressure gradient across valve during systole as well as LV size and function
157
What is classified as severe aortic stenosis?
Valve area <1cm squared
158
What is the management for people with aortic stenosis?
1. IE prophylaxis in medical and dental procedures
2. Vasodilators relatively contraindicated if severe
3. Surgical replacement
4. TAVI (transcutaneous aortic valve implantation)
159
What are the indications for aortic valve replacement in individuals with aortic stenosis?
1. Symptomatic patients with severe
2. Patients with severe AS undergoing CABG or surgery on aorta or other valves
3. Patients with severe AS and depressed LVEF
OR/ in absence of symptoms: if valve area <= 0.6cm squared or if valve gradient exceeds 50mmHg on echo
160
What is mitral regurgitation?
Backflow of blood from LV to LA during systole
161
What are the most common causes of mitral regurgitation?
1. In developed world - prolapsing mitral valve (myxomatous degeneration)
2. In developing world - rheumatic heart disease
3. Infective endocarditis
162
How does mitral regurgitation often present?
Pulmonary oedema, due to pulmonary hypertension from increased pressure in left atrium.
Pulmonary hypertension can cause LV hypertrophy and LA enlargement in attempt to compensate, however often pulmonary hypertension will lead to right heart failure --> heart failure
163
What are the physical signs on examination of an individual with mitral regurgitation?
1. Soft S1, with pansystolic murmur (fills all of systole) at the apex and radiating into axilla
2. Apex beat displaced laterally
3. S3 often present
4. Exercise intolerance (dyspnoea on exertion)
5. HF
164
Where do you auscultate all valves?
Aortic - Right 2nd intercostal space (sternum)
Pulmonary - Left 2nd intercostal space (sternum)
Tricuspid - Left 4th intercostal space (sternum)
Mitral - Left 5th intercostal space mid clavicular line
165
What is rheumatic fever?
Inflammatory disease that occurs in children and young adults as a result of infection with group A B haemolytic streptococci. This causes an autoimmune reaction, and can impact heart valves.
166
How does rheumatic heart disease present both clinically and on examination?
1. 2-3 weeks after sore throat, acute onset
2. Fever
3. Joint pain
4. Loss of appetite
On examination
1. Changing heart murmurs/chest pain
2. Polyarthritis
3. Skin - erythema marginatum (transient pink rings) as well as small nodules over joints
4. Sydenham's chorea - Fidgety and sposmodic unintentional movement- involvement of CNS
167
What criteria is used in the diagnosis of rheumatic fever?
Duckett Jones criteria
168
What treatment is given in rheumatic fever?
1. Bed rest
2. High dose aspirin
3. Penicillin to eradicate infection and long term to any with persistent damage
169
What do splinting haemorrhages suggest?
Endocarditis
170
What compensatory mechanisms does the body use in HF to maintain CO and peripheral perfusion?
1. Increased sympathetic tone - improves ventricular function by increasing heart rate and contraction. It also contricts venous capacitance vessels meaning increased venous return to heart (preload) which further augments ventricular function (Starling)
2. Fall in CO and increased sympathetic tone = diminished renal perfusion and activation on renin-angiotensin system and therefore increased fluid retention, which further increases venous pressure and maintains stroke volume.
171
Why is oedema often seen in cardiac failure?
A fall in CO and increased sympathetic tone (which both occur in HF) leads to decreased renal perfusion and therefore activation of renin angiotensin system. This promotes sodium and water retention which in turn increases venous pressure and fluid retention.
172
What are the two main differential diagnoses of DVT?
Cellulitis or HF
173
What is the clinical presentation of DVT?
Pain, swelling, tenderness, warmth, discolouration
174
What is the initial investigation carried out in suspected DVT? What is its significance?
D-dimer
Used for exclusion only - if normal: excludes DVT as can be raised in operation, pregnancy, inflammation.
175
What is D-dimer test looking for in DVT?
Breakdown products of fibrin
176
What things other than a clot can cause a D-dimer test to be raised?
Pregnancy, inflammation, operation
177
If D-dimer came back raised in suspected DVT what would be the next investigation done?
Ultrasound compression test
178
Ultrasound in DVT is the second investigation done after D dimer. In what case is the ultrasound useless?
If DVT is sitting in the calf. If they return a week later is likely to have moved proximally.
179
What are the main risk factors for DVT?
1. Surgery/immobility/leg fracture/POP
2. OC pill, HRT, pregnancy (hypercoaguable in last trimester)
3. Long haul flights/travel
4. Inherited thrombophilia
180
What is the treatment for a patient with confirmed DVT?
1. LMW Heparin (s/c for min 5 days)
2. Oral warfarin (DOAC) for 6 months if unclear cause, and 3 months if clear cause
3. Compression stocking
4. Treat underlying cause (if there is one)
181
What is the difference in the length of time that oral warfarin is prescribed after a DVT when the cause is known compared to when the cause is unknown?
Cause known = 3 months
| Cause unknown = 6 months
182
In what groups of people in hospital should thromboprophylaxis be considered?
Hip and knee, pelvis, malignancy, prolonged immobility
183
What are the signs and symptoms of PE?
and massive PE?
Pleuritic chest pain, breathlessness, signs of DVT sometimes, (risk factors), tachycardia, pleural rub, tachypneoa
Massive PE: hypotension, cyanosis, severe dyspnoea, right heart failure
184
What are the initial investigations done in suspected PE?
And the gold standard further investigation (used to diagnose)
1. CXR - abnormal in pneumonia, pneumothorax
2. ECG - sinus tachy
3. Blood gas - Type 1 resp failure (decreased Co2 and o2)
Gold standard = CTPA (pulmonary angiogram)
185
What are the differential diagnosis of PE?
Lung cancer, pneumothorax, reflux, chest infection, musculoskeletal
186
What is the treatment for PE?
Same as DVT:
1. LMW Heparin (s/c for min 5 days)
2. Oral warfarin (DOAC) for 6 months if unclear cause, and 3 months if clear cause
3. Compression stocking
4. Treat underlying cause (if there is one)
187
Define population atrributable factor (PAF)
The proportion of the incidence of a disease in an exposed and non-exposed ppn that is due to an exposure, i.e. the disease incidence in the population that could be eliminated if the exposure were eliminated.
188
What are the two biggest risk factors for CHD?
Cholesterol ratio ApoB/ApoA1
| Smoking
189
There are 2 main philosophical standpoints in explaining the pattern of CHD and who is affected by it. What are they called and outline their principles.
1. Absolutist explanations e.g. Townsend score
- It is about poverty and absolute measures of socioeconomic deprivation
2. Relativist explanations e.g. Richard Wilkinson- Spirit Level
- It is about relative differences, the larger the relative differences in society the poorer the outcomes and worse off for all e.g. infant mortality rates are higher in countries with high income inequality
190
What is the effect of type A/B personality on the risk of CHD? Back this up with studies.
Type A:B 2:1 risk of CHD, found in both the Western collaborative group study and the Framington heart study
191
What aspect of a Type A personality has been suggested to be the key risk factor in CHD?
Hostility
192
What psychosocial job characteristics are associated with MI? What study backs this up?
High demand and low control
Whitehall studies - men in lowest grades had higher CHD risk
193
What psychosocial factors could influence risk of CHD?
1. Personality type (A/B)
2. Work characteristics (over 11 hour days/ high demand and low control)
3. Depression/anxiety
4. Low social support
194
Give 3 causes of left axis deviation
Often issue with LAD
- LBBB
- Left anterior fascicular block
- Left ventricular hypertrophy
195
Give 3 causes of right axis deviation
- Left posterior fascicular block
| - Right heart hypertrophy/strain
196
T wave flattening or inversion is seen in?
Ischamia or hours after onset of STEMI
197
If STEMI was inferior, what leads would it be seen in ?
II, III aVF
198
If STEMI was septal what leads would it be seen in?
V1, V2
199
Anterior infarct would be seen in leads?
V2-V6
200
Lateral infarct would be seen in leads?
I, II, aVL
201
What investigations would be done in suspected STEMI?
CXR, FBC, U&E, blood glucose and lipids, Cardiac markers (Troponin T and I and CK MB)
202
What are the ECG changes in hyper and hypokalemia?
Hyper- Tall T waves, flattening of P waves, broadening of QRS
Hypo- Flattening of T wave and QT prolongation
203
What are the ECG changes in hyper and hypocalcaemia?
Hyper - QT shortening
| Hypo - QT prolongation
204
What is the most common congenital heart defect?
Ventricular septal defect
| Then ASD, PDA
205
Is VSD a cyanotic or acyanotic CHD? and why
Acyanotic - High pressure LV and low pressure RV so blood flow from left to right --> increased blood flow through lungs
206
VSD can lead to what?
Eisenmengers
207
If VSD is small, what sign is still often present?
Loud systolic murmur and thrill
208
Give 3 signs of a large VSD in an infant
Breathless, failure to thrive, poor feeding, large heart on xray, increased RR, tachycardia
209
What is Eisenmengers?
Seen in VSD if large and left untreated. There is high pressure pulmonary blood flow, which leads to damage in pulmonary vasculature leading to increased resistance in the lungs
RV pressure then increases and shunt reverses
Child becomes cyanotic
210
Give two examples of cyanotic CHDs?
Tetralogy of Fallot, Eisenmengers
211
Give two examples of acyanotic CHD's?
Ventricular septal defect, atrial septal defect
212
ASD often presents in what age?
Adulthood
213
VSD often presents in what age group?
Infants
214
How do you treat a small ASD?
You don't - leave (no symptoms)
215
Signs of ASD?
1. RH dilatation (big on xray)
2. SOBOE
3. Increased susceptibility of chest inf.
4. Pulmonary flow murmur
5. Fixed split second heart sound
6. Big pulmonary arteries on CXR
216
AVSD are often seen in patients with what disease?
Downs
217
What is the malformation seen in AVSD?
One big malformed AV valve (rather than 2)
218
How does an infant with AVSD present?
Breathless, failure to thrive, poor feeding and weight gain
219
What are the 4 features typical of ToF?
1. Overriding aorta
2. Pulmonary stenosis
3. Hypertrophy of R ventricle
4. VSD
220
What is the gene deletion that leads to ToF?
22q11
221
ToF is normally resolved by what age?
2y
222
Severity of illness in ToF greatly depends on what?
Severity of pulmonary stenosis - stenosis of RV outflow leads to RV being at higher pressure than the left --> cyanotic
223
What is seen on CXR of patient with ToF?
Boot shaped heart
224
What investigation is used to determine severity of stenosis in ToF?
Echo
225
Give 3 clinical signs seen in ToF?
1. Toddlers squat - increases PVD so degree of shunt reduced
2. Difficulty feeding, failure to thrive and clubbing
3. Adult patient - cyanosis
226
What signs would indicate that patient required re-do surgery for TofF?
1. Exertional dyspnoea
2. Palpitations
3. RV failure
4. Syncope
Note/ can lead to sudden death
227
In what direction is the shunt in PDA?
L--> R
228
PDA is very common in what group of people?
Preterm babies
229
What kind of murmur is heard in PDA?
Continuous 'machinery' murmur
230
How does a baby with PDA appear?
Breathless, poor feeding, failure to thrive
231
How is PDA treated?
Surgical or percutaneous closure
232
What is coarctation of the aorta?
Narrowing of aorta at site of entry of ductus arteriosus
233
What is the major complication in a severe coarctation of aorta?
Extreme HF --> death
234
What are the clinical signs seen in coarctation of aorta?
Right arm hypertension
Bruits (buzzes)
Murmur
235
Why are bicuspid AV valves an issue?
1. Degenerate faster than normal valves
2. Can be severely stenotic
3. Associated with coarctation and dilation of ascending aorta
236
What is pulmonary stenosis?
Narrowing of outflow of RV
237
How does severe pulmonary stenosis present?
1. RV failure as neonate
2. RV hypertrophy
3. Poor pulmonary blood flow
4. Tricuspid regurg
238
What is the Rx in pulmonary stenosis?
1. Balloon valvuloplasty
2. Open valvotomy
3. Shunt
239
Digoxin is indicated in which conditions?
HF + AF
OR HF (severe)
240
How does digoxin work (mechanism)?
Inhibits Na/K pump
241
What effects does digoxin have on body?
1. Bradycardia
2. Slows AV conduction
3. Increases no. of ectopics
4. Increases inotropic response
242
Give 2 side effects of digoxin
1. Nausea and vomiting
2. Diarrhoea or constipation
V narrow therapeutic range
243
What two drugs often cause QT prolongation and polymorphic ventricular tachycardia?
Amiodarone, sotalol
244
Give 5 side effects of amiodarone
1. Multiple drug interactions
2. Interstitial pneumonitis
3. Slate grey skin and sensitivity to sun
4. Corneal microdeposits and optic neuropathy
5. Hyper/hypothyroid
6. Abnormal LFT
And very large volume of distrubution
245
What is the difference between intermittent claudication and critical leg ischaemia?
Intermittent claudication - Pain on exertion, it is a moderate ischaemia often described as muscle cramp in the calf area. There is anaerobic metabolism when O2 demand exceeds supply. Lactic acid is formed and there is pain distal to atheroma.
Critical ischaemia - Pain at rest, typically lower down leg than calf. Often described as nocturnal and patient at risk of gangrene. There is dependency rubor. Blood supply is barely adequate to allow basal metabolism.
246
What are the 6 P's of acute ischaemia?
Pain, pale, pulseless, paraesthesia, paralysis, perishing cold
247
What are the 4 stages of chronic limb ischaemia?
1. Asymptomatic
2. Intermittent claudication
3. Rest pain/nocturnal pain
4. Gangrene
248
Briefly outline management of peripheral vascular disease (3 steps)
1. Risk factor modification
2. Revascularisation (vein bypass, percutaneous balloon angioplasty, stenting)
3. Amputation
249
Mechanism of streptokinase?
Plasminogen activator
250
Investigations in suspected PVD?
History and examination
Ultrasound
Angiogram
251
Most common causes of heart block?
1. Coronary artery disease
2. Cardiomyopathy
3. Fibrosis of conducting tissue
252
Difference in content of arterial and venous blood? - to do with drugs working there
Arterial - platelet rich (use antiplatelets)
| Venous - fibrin rich - (use anticoag.)
253
Mechanism of heparin?
Binds to antithrombin and increases activity
254
How are mechanisms of aspirin and clopidogrel different?
Aspirin - Cox inhibitor, meaning that thromboxane production is inhibited, and hence there is platelet aggregation
Clopidogrel - inhibits ADP induced platelet aggregation
255
How do NOAC's work?
Work similarly to warfarin - Inhibit factors II and X
